Tissue- and subunit-specific regulation of G-protein expression by hypo- and hyperthyroidism

Michel-Reher, Martina B.; Groß, Gerhard; Jasper, Jeffrey R.; Bernstein, Daniel; Olbricht, Thomas; Brodde, Otto‐Erich

doi:10.1016/0006-2952(93)90040-4

Cited by 31 publications

(11 citation statements)

References 21 publications

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“…In our own studies we have previously reported Gprotein alterations in erythrocytes and platelets of adult HD and CAPD patients [8], but their regulation may depend on cell type rather than mode of dialysis. This is in good agreement with a large body of data indicating that within a given animal regulation of G-protein expression by, e.g., thyroid hormone [15] or arterial hypertension [9,10], also occurs in a tissue-dependent manner. In the present study a similar platelet expression of α-subunits of G i2 , G i3 , G s long and G s short was observed in HD and control children.…”

Section: Discussionsupporting

confidence: 91%

Platelet adenylyl cyclase signaling remains unaltered in children undergoing hemodialysis treatment

Keffel

Bonzel

Wingen

et al. 2001

Pediatric Nephrology

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Patients with chronic renal failure exhibit multiple endocrine, gastrointestinal and cardiovascular abnormalities, many of which may be explained by alterations of adenylyl cyclase (AC) responsiveness and/or G-protein expression. Since such alterations were previously reported, e.g., for platelets of adult chronic renal failure patients undergoing hemodialysis treatment (HD), we have investigated whether children with chronic renal failure undergoing HD exhibit similar alterations. Eleven uremic children undergoing HD were compared with 11 age-matched healthy controls. Platelet AC activity was determined in the absence (basal) and presence of a receptor agonist, direct G-protein activators and direct AC stimulators. G-protein alpha-subunits were measured by quantitative immunoblotting. Basal and stimulated platelet AC and immunoreactivity for platelet G-protein alpha-subunits did not significantly differ between HD and control children. We conclude that HD in children is associated with much smaller, if any, abnormalities of blood cell signal transduction than in adult patients. We speculate that quality of dialysis, age, and underlying disease might differentially influence blood cell signal transduction cascades.

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Section: Discussionsupporting

confidence: 91%

Platelet adenylyl cyclase signaling remains unaltered in children undergoing hemodialysis treatment

Keffel

Bonzel

Wingen

et al. 2001

Pediatric Nephrology

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“…Pertussis toxin-catalyzed ADP-ribosylation was assessed under conditions yielding maximal ribosylation as previously described 16 with minor modifications. 14 Briefly, cell membranes were incubated with 1 jtmol/L f^PJnicotinamide adenine dinucleotide (NAD) and 0.2 fig pertussis toxin for 1 hour at 30°C. The ribosylation reaction was stopped by addition of sample buffer (4% SDS, 20% gh/cerol, 10% 2-mercaptoethanol, 125 mmol/L Tris-HCl, pH 8.0) and subsequent boiling.…”

Section: Adp-ribosylationmentioning

confidence: 99%

Ontogenesis of sympathetic responsiveness in spontaneously hypertensive rats. II. Renal G proteins in male and female rats.

et al. 1994

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Previously we have reported an increased renal a,-and /3-adrenergic receptor expression in male spontaneously hypertensive rats that occurred ontogeneticalry in parallel with blood pressure elevation. However, increased receptor numbers were not accompanied by enhanced stimulation of inositol phosphate and cyclic AMP formation, respectively, indicating relative desensitization. We have now quantified a-subunits of the G proteins G, (G, ,,"," and G, t^), G,, and G q by immunoblotting and pertussis toxin-catalyzed ADP-ribosylation in renal membranes from 3-, 6-, 8-, and 28-week-old normotensive and spontaneously hypertensive male WistarKyoto rats; additionally, 28-week-old female normotensive and spontaneously hypertensive rats were studied. During ontogenesis of male normotensive rats, G, &" increased, G, r emained unchanged, and G^ and G,,, decreased. In adult normotensive rats no sex differences were detected for G, ^^, G, k.,, and G^. When male rats from the normotensive and T he kidney is the tissue with the greatest long-term impact on blood pressure control because of its infinite gain mechanism. 1 On the other hand, chronically elevated arterial blood pressure affects renal function.2 -3 Renal function is tightly controlled by neurotransmitters and hormones such as catecholamines, angiotensin II, endothelin, vasopressin, and neuropeptide Y, many of which act via G proteins. -6 We have recently reported that in parallel with blood pressure elevations numbers of a t -, a 2 -, and /3-adrenergic receptors increase in kidneys of spontaneously hypertensive rats (SHR) relative to those of age-matched normotensive Wistar-Kyoto (WKY) rats.7 Despite increased a r and /3-adrenergic receptor numbers, norepinephrine-stimulated inositol phosphate formation and isoprenaline-stimulated cyclic AMP (cAMP) formation remained unchanged.7 These data suggest the occurrence of a relative desensitization of renal a r and £-adrenergic receptors during the development of hypertension in SHR./3-Adrenergic receptor coupling to cAMP formation by adenylate cyclase occurs via the stimulatory G protein G, and can be attenuated via the inhibitory G protein G ; .8 aj-Adrenergic receptor coupling to inositol phosphate formation appears to occur via G q and/or G n 9 ; additionally, one or more subtypes of a^-adrenergic receptors may couple to inositol phosphate formaReceived October 21, 1993; accepted in revised form January 24, 1994.From the Department of Medicine, University of Essen, Germany.Correspondence to Dr Martin C. Michel, Nephrol. Lab. IG 1, Klinikum, Hufelandstr 55, D-45122 Essen, Germany. spontaneously hypertensive strains were compared, all G protein a-subunits were similar in the prehypertensive phase (3 weeks). In established hypertension (28 weeks), G, ,"", and G,,, were reduced, whereas G, &,« and G^ remained unchanged. G, fco, was also reduced during the development of hypertension (6 and 8 weeks), whereas G, ^ and G^, were not consistently altered in this phase. The reduction in G, ^^ seen in male adult hypertens...

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“…The blots were washed twice with TTBS for 10 min. Detection of the primary antibodies was performed with [ 125 I]‐protein A (polyclonal anti‐sera) as described by Michel‐Reher et al (1993) or with the ECL system (monoclonal antibodies) according to the manufacturers instructions.…”

Section: Methodsmentioning

confidence: 99%

Protein kinase C isoenzymes in rat and human cardiovascular tissues

Erdbrügger

Keffel

Knocks

et al. 1997

British J Pharmacology

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1 We have compared the expression of protein kinase C (PKC) activity and immuno-detectable isoenzymes in cytosolic and membrane extracts of rat and human cardiovascular tissues (heart, kidney, aorta, saphenous vein). Experiments were performed in raw extracts and upon combined diethylaminoethylcellulose (DEAE) and phenylsepharose column chromatography. 2 PKC activity that bound to DEAE mostly eluted with 200 mM NaCl. DEAE-puri®ed PKC from all tissues except rat kidney bound almost quantitatively to phenylsepharose and eluted with 0.5 ± 0 M NaCl. 3 Immunoblots with an antibody against classical PKCs and the activator pro®le for phosphatidylserine, diolein and Ca 2+ revealed that the PKC from rat kidney, which did not bind to phenylsepharose, was most probably due to a proteolytically-generated, constitutively active PKC which is not under the control of a regulatory subunit. 4 Studies in the reference tissue, rat brain, demonstrated that all PKC isoenzymes investigated (classical PKCs a, b, g, new PKCs d, e, Z, y, and atypial PKCs z, l, i) have similar DEAE and phenylsepharose chromatography elution pro®les. In the functional assay an inhibitor of all known PKC isoenzymes, bisindolylmaleimide, and a speci®c inhibitor of classical PKCs, GoÈ 6976, both inhibited PKC from rat brain completely and with high potency indicating that the functional assay preferentially detects classical PKC isoenzymes. 5 Each PKC isoenzyme had a tissue-speci®c expression pro®le which was similar in rat and man. The classical PKCa, the new PKCs d and e and all atypical PKCs were detectable in most tissues, whereas the PKCb and PKCg were not detected in any pheripheral tissue; PKCZ and PKCy were found in some tissues. 6 We conclude that combined DEAE and phenylsepharose chromatography is useful to enrich and detect PKC isoenzymes; no major species dierences in tissues-speci®c expression patterns appear to exist between rat and man.

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Tissue- and subunit-specific regulation of G-protein expression by hypo- and hyperthyroidism

Cited by 31 publications

References 21 publications

Platelet adenylyl cyclase signaling remains unaltered in children undergoing hemodialysis treatment

Platelet adenylyl cyclase signaling remains unaltered in children undergoing hemodialysis treatment

Ontogenesis of sympathetic responsiveness in spontaneously hypertensive rats. II. Renal G proteins in male and female rats.

Protein kinase C isoenzymes in rat and human cardiovascular tissues

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